Limbic seizures originating in the olfactory bulb: an electro-behavioral and glucose metabolism study

We studied seizures which were induced by a microinjection of kainic acid (KA) into the unilateral olfactory bulb (OB) in the rats. The first epileptiform discharge appeared in the OB, was then propagated to the amygdala and the hippocampus unilaterally, and finally propagated to the unilateral sensori-motor cortex. Consistent graded behavioral changes, almost identical to those of the amygdaloid and hippocampal seizures, occurred during the development of the seizures, and three stages were classified: stage 1 was staring, stage 2 consisted of masticatory movement and stage 3 demonstrated rearing and rearing and falling. Local cerebral glucose utilization (LCGU) measured with the [14C]2-deoxyglucose method revealed a graded propagation of seizure activities at each stage in the unilateral structures. At stage 1, the increased activities propagated from the OB localized in the anterior olfactory nucleus; at stage 2, the endopiriform nucleus, the nucleus accumbens, the entorhinal cortex, the ventral globus pallidus and the globus pallidus were all activated; at stage 3, the thalamic nuclei (mediodorsal, ventrolateral, ventromedial and centromedian nuclei), the substantia nigra pars reticulata, the entopeduncular nucleus and the sensorimotor cortex were also activated. The globus pallidus, which receives afferent fibers from the nucleus accumbens, was the first structure that was activated metabolically among the extralimbic structures. No metabolic activation occurred in the amygdala and the hippocampus in spite of the early propagation of epileptiform discharges to these structures on EEG. These results suggest that OB seizures involve the limbic structures, while the amygdala and the hippocampus have a little contribution to OB seizures. In addition, the nucleus accumbens plays an important role as a functional interface between the limbic and the motor system in OB seizures.